This disclosure relates generally to monitoring of electrocardiograms in patient monitors. More particularly, the present invention relates to prediction of ventricular tachyarrhythmias (VTAs) in patient monitors.
Patient monitors are electronic devices designed to display physiological information about a subject. Electrocardiogram (ECG), electroencephalogram (EEG), plethysmographic signals, and signals related to blood pressure, temperature, and respiration represent typical physiological information contained in full-size patient monitors. Patient monitors are typically also furnished with alarming functionality to alert the nursing staff when a vital sign or physiological parameter of a patient exceeds or drops below a preset limit. Alarms are normally both audible and visual effects aiming to alert the staff to a life-threatening condition or to another event considered vital. In most monitors, the alarm limits may be defined by the user, since the limits typically depend on patient etiology, age, gender, medication, and various other subjective factors. Each specific physiological parameter, such as heart rate or blood pressure, may also be assigned more than one alarm limit. Furthermore, there is a lot of data trended and available for caregivers to be reviewed in a patient monitor.
For recording an electrocardiogram, electrocardiographic leads are used at specified locations of the subject for recording ECG waveforms. In typical clinical practice, 12 leads are used to the record the ECG. However, the number of leads used may vary. Each lead records a waveform representing the electrical activity generated by the heart cardiac cycle by cycle and together the lead recordings provide spatial information about the heart's electrical activity.
A normal cardiac cycle includes contractions of the atrial muscles, which are activated by the autonomic sinoatrial node (SA node), also called the sinus node. An electrophysiologic (EP) signal generated by the SA node spreads in the right and left atrium leading to their contraction. The EP signal further reaches the atrioventricular node (AV node) situated between the atria and the ventricles. The AV node delays the EP signal, giving the atria time to contract completely before the ventricles are stimulated. After the delay in the AV node, the EP signal spreads to the ventricles via the fibers of the His-Purkinje system leading to the contraction of the ventricles. After the contraction, the atria are relaxed and filled by blood coming from venous return. The entire cardiac cycle is a combination of atrial and ventricular contractions, i.e. depolarizations, and relaxations, i.e. repolarizations.
Cardiovascular disease is currently the most common single cause of natural death in developed countries. Sudden cardiac death (SCD) is estimated to account for approximately 50 percent of these deaths. Ventricular tachyarrhythmias (VTAs) are thought to be the most common primary cause of SCD and also the most dangerous heart rhythm disturbances. Ventricular tachyarrhythmias refer to tachycardias, or fast heart rhythms, that originate from lower ventricles of the heart. Ventricular tachyarrhythmias include ventricular tachycardia (VT) and ventricular fibrillation (VF). Prolonged ventricular arrhythmias may lead to a completely pulseless state called asystole (ASY).
Mechanisms of ventricular tachyarrhythmias are known and rather well studied. The ultimate cause of a ventricular tachyarrhythmia is a critical alteration in the electrical properties of cardiac myocotes. Due to this, the electrical activation does not originate from the AV node and/or does not propagate in the ventricles in a normal way. Although the arrhythmogenic mechanisms are rather well known, the onset of ventricular tachyarrhythmia is not known. It may, however, be assumed that the mechanoelectric properties of the myocardium are altered prior to the onset. In recent years, various morphology related parameters and variability parameters, i.e. parameters related to the alterations and variability of heart beats, have been studied to find prognostic parameters for imminent ventricular tachyarrhythmia events. For example, multiple studies have been conducted to discover whether a spontaneous initiation of VTA and increased T wave alternans (TWA) have a causal relationship. These studies show, for example, increased TWA that peaks about 10 minutes before the onset of a VTA event. Despite the studies conducted, reliably precursors of VTAs have not been found, which is a manifestation of the complexity involved. In general, current research on precursors of VTAs is still in a rather disorganized and immature state that may be characterized by small sizes of databases that are not publicly available, by findings that are not independently reproduced, and by methods that are not clearly documented and standardized. Therefore, no technology exists at present for predictive VTA algorithms, but current patient monitors are able to detect VTA events only when they occur. This is a significant drawback since when a lethal arrhythmia occurs it may take up to several minutes before a rescue team is in position to start the resuscitation procedures. In this situation every second counts as damage to organs is most probably already occurring. It is estimated that the survival probability of a VTA patient decreases 7 to 10 percent with every minute of treatment delay.
Consequently, current patient monitor technology is not able to anticipate an imminent VTA event but can alert the nursing staff only when a VTA event is a reality. Reliable prediction of imminent VTA events would, however, greatly improve the survival chances of the patient, especially as efficient treatments, such as defibrillation, are commonly available.